Vitamin cycles such as the folic acid and homocysteine cycle are essential regulators of cell alignment, orientation, and development of the neural tube. If there is too little folic acid or too much homocysteine, then the neural tube will develop malformations. Neural tube defects still occur despite attempts to supplement mothers with folic acid, due to late supplementation or deficiencies in folic acid uptake. As a result, children are born with deformed spines, or pieces of their skull are missing. One of the most severe neural tube defects is spina bifida (SB). This neural tube defect affects the lumbar region of the back which innervates the bladder. Due to this disruption of innervation, when children are born, they do not have proper control of their lower bodies, especially their bladders. The improper neurological connection in SB patients leads to the development of neurogenic bladders. As soon as children affected by SB are born, their bladders are catheterized. The children cannot sense when they need to void their bladder and do not have proper control of it. The children do not have proper urological control because the extracellular matrix of the neurogenic bladder contains excess elastin and insufficient collagen. It has been shown that homocysteine can upregulate collagen production and degrade elastin networks. I study, the effect of homocysteine and folic acid on the extracellular matrix of bladder smooth muscle cells. This is done by culturing rat bladder smooth muscle cells on a pre-stretched polydimethylsiloxane surface to model a SB neurogenic bladder. In addition, the growth rate of the smooth muscle cells and their alignment are evaluated on the pre-stretched surface. We hypothesize that this model would allow us to investigate the effect of homocysteine and mechanical cue on the extracellular matrix of the bladder smooth muscle cells.